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The population dynamics of a bacterial pathogen after host re-infection affects the founding population size
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In natura, many organisms face multiple infections by pathogens. The ability of a pathogen to reinfect an already-infected host affects the genetic makeup of the pathogen population at the end of the infectious cycle. Despite the likely prevalence of this situation, the population dynamics of pathogens during multiple infections over time is still poorly understood. Here we combined theoretical and empirical investigations of the founding population size, a critical driver of the evolution of pathogens, in a setting allowing for multiple and subsequent re-infections. Using the soil-borne bacterial pathogen Ralstonia solanacearum and tomato as its host, we first assessed the strength of the host infection bottleneck, and showed that both the host barrier and the immune system work additively to constrain the infection. Then, by increasing the temperature, we experimentally demonstrated that the increased pathogen proliferation within the host reduces the contribution of subsequent re-infection leading to a lower founding population size. Our study highlights the importance of within-host pathogen proliferation in determining founding population size – and thus bacterial genetic diversity during epidemics – for pathosystems where multiple re-infections occur. Under current global changes, our work notably predicts that an increased temperature provided this increase has a beneficial impact on pathogen growth, should decrease the founding population size and as a consequence potentially lower the diversity of the infecting and transmitted pathogen population. Significance Statement Founder population size is a major determinant of pathogen evolution, yet we still have limited insights into effective populations in natural settings. Most studies have considered infection as a single event, followed by pathogen growth in the host. But, in natura, organisms typically face multiple infections by several co-exisiting pathogen strains. Therefore, effective population size will depend on the timing and relative growth rate of the different infecting strains. In this work, we predict and experimentally show that both priority effects and within-host competition determines effective founding size, with an over-contribution of fast-growing and early infecting genotypes. This work sheds a new light on the ecological and evolutionary pressures affecting infection dynamics in realistic conditions.
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